Department of Oral Biology & Diagnostic Sciences: Student Research and Publications

Permanent URI for this collectionhttps://hdl.handle.net/10675.2/622145

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Now showing 1 - 5 of 5
  • ItemOpen Access
    Influence of Porphyromonas gingivalis on Anti-Apoptotic/Autophagic Signaling Pathways in Human Dendritic Cells
    (Augusta University, 2019) Meghil, Mohamed; Tawfik, Omnia; Elashirty, Mahmoud; Rajendran, Mythilypriya; Arce, Roger; Schoenlein, Patricia V.; Cutler, Christopher; Department of Oral Biology & Diagnostic Sciences, Department of Periodontics, Department of Cellular Biology and Anatomy
    The purpose of this study was to investigate the molecular mechanisims of P. gingivalis-mediated disruption of homeostatic apoptosis and autophagy in DCs.
  • ItemOpen Access
    Innate Lymphoid Cells in Periodontitis: A Novel Therapeutic Modality
    (Augusta University, 2019) Ghaly, Mira; Emami, Golnaz; Khodadadi, Hesam; Mozaffari, Mahmood; Baban, Babak; Department of Periodontics, Department of Oral Biology and Diagnostic Sciences
    To determine the presence of ILCs in human periodontium which are emerging immune cells with the potential to be targeted, via novel therapies, in the treatment of peridontitis.
  • ItemOpen Access
    Proliferative Verrucous Leukoplakia (PVL) Expresses High Levels of Toll-Like Receptor 2 (TLR2)
    (Augusta University, 2019) Koh, Joon; Kurago, Zoya; Georgia Cancer Center
    In the current study, we analyzed samples of human oral mucosal PVL and other epithelial disorders to test the possibility that, if TLR2 is involved in early stages of carcinogenesis, then keratinocytes in early-intermediate stages of PVL may express more TLR2 than keratinocytes in non-dysplastic epithelium.
  • ItemOpen Access
    Phosphorylation of EPS8 Mediates Its Downstream Signaling and Biological Functions
    (Augusta University, 2019) Shahoumi, Linah; Yeudall, W. Andrew; Department of Oral Biology & Diagnostic Sciences, Georgia Cancer Center
    The purpose of this study was to investigate the role of EPS8 phosphorylation in modulating biochemical signaling, cell proliferation and motility in HNSCC.
  • ItemOpen Access
    Histology of the Dental Extraction Sites of Bisphosphonate Treated Rats
    (Augusta University, 2018-12) Ferguson, Alisa; Department of Oral Biology and Diagnostic Sciences
    Bisphosphonate is a drug given to both men and women who are experiencing decreasing bone density and strength. When patients taking bisphosphonate undergo some sort of jaw trauma (i.e. tooth extraction, accident), they can experience necrosis or cell death of the jawbone. Our hypothesis is that bisphosphonate molecules bound to the bone matrix contribute to bone necrosis. For my thesis, a histological analysis of the mandibles from bisphosphonate treated rats after dental extraction with and without removal of bisphosphonates from the extraction site of the bone was done. Histological sections of the jaw from bisphosphonate treated rats after bilateral extraction of the first and second molar teeth were taken. On one side, the extraction site was treated with EDTA to chelate bisphosphonates from the bony wall of the tooth socket. The other side of the rat’s jaw was treated with Saline. I then evaluated the vitality of alveolar bone by counting the number of dead versus live osteocytes around the extraction site and comparing the ratios between the chelated and un-chelated sides from each rat. The study determined whether removal of localized bisphosphonates is beneficial to preserve bone vitality after dental extraction. As expected, the percentage of live osteocytes decreased in the alveolar bone of animals treated with Zoledronate (ZA), a strong dose of bisphosphonate. Furthermore, there was a trend of increased percentage of live cells when EDTA was used, although the differences were not statistically significant. These results support other studies in our laboratory that have shown that localized bisphosphonates play a role in the osteonecrosis associated with ZA treatment. It, therefore, provides evidence that localized bisphosphonates contribute to the etiology of bone necrosis in patients undergoing bisphosphonate treatment.